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Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [Cut&Tag]

ABSTRACT: Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [Cut&Tag]

PROVIDER: PRJNA744056 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15048143_1.fastq.gz	Fastqsanger.gz
	SRR15048143_2.fastq.gz	Fastqsanger.gz
	SRR15048144_1.fastq.gz	Fastqsanger.gz
	SRR15048144_2.fastq.gz	Fastqsanger.gz

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Brd4 regulates the homeostasis of CD8+ T-lymphocytes and their proliferation in response to antigen stimulation [Cut&Tag]

Project description:CD8+ T cells are major components of adaptive immunity and confer robust protective cellular immunity, which requires adequate T-cell numbers, targeted migration, and efficient T-cell proliferation. Altered CD8+ T-cell homeostasis and impaired proliferation result in dysfunctional immune response to infection or tumorigenesis. However, intrinsic factors controlling CD8+ T-cell homeostasis and immunity remain largely elusive. Here, we demonstrate the prominent role of Brd4 on CD8+ T cell homeostasis and immune response. By upregulating Myc and GLUT1 expression, Brd4 facilitates glucose uptake and energy production in mitochondria, subsequently supporting naïve CD8+ T-cell survival. Besides, Brd4 promotes the trafficking of naïve CD8+ T cells partially through maintaining the expression of homing receptors (CD62L and LFA-1). Furthermore, Brd4 is required for CD8+ T cell response to antigen stimulation, as Brd4 deficiency leads to a severe defect in clonal expansion by decreasing glycolysis. Importantly, as JQ1, the specific inhibitor of Brd4, severely dampens CD8+ T-cell immune response, its usage as an anti-tumor agent or latency-reversing agent for human immunodeficiency virus type I (HIV-1) should be more cautious. Collectively, our study identifies a previously-unexpected role of Brd4 in the metabolic regulation of CD8+ T cell-mediated immune surveillance and also provides a potential immunomodulation target.

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Targeting BRD4 Ameliorates Experimental Emphysema Via Suppressing both M1 and M2 alveolar macrophage polarization-3 [CUT&TAG]

Project description:BRD4 inhibition suppressed M2 macrophage polarization. Particularly, we deeply investigated the underlying molecular mechanism of how BRD4 epigenetically regulate M2 genes expression. And finished the cut&tag experiment using BRD4, H3K27ac, IRF4 as antibody to find out the binding sites change in M2 macrophage treated with ARV825.

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Project description:We performed multiomic high-throughput sequencing to recapitulated the primary mechanism of mesenchymal stem cells osteogenesis. We analysed the H3K27ac ChIP-seq, BRD4 CUT&Tag and RNA-seq data before and after osteogenesis, and identified super enhancers (SEs) regulated osteogenic identity genes in MSCs.

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